There is a general consensus that the aetiology of eating disorders
is multidetermined, affected by biological, psychological and social
factors that interact in a complex fashion (Garfinkel, Kennedy and
Kaplan, 1995). And while it is clear that no one cause for eating
disorders will be discovered, the role of the central nervous system
(CNS) deserves special attention as the CNS must play a central
role in mediating and maintaining eating behaviours. A fuller
understanding of CNS control of eating may lead to improvements
in the medical treatment of various disorders of eating. For these
reasons, direct and non-invasive analytic methods of brain imaging
are now widely applied in the study of eating disorders (Ellison and
Foog, 1998; Krishnan and Gadde, 1998; Grady, 1999; Demaerel,
2000; Hendren, De Backer and Pandina, 2000).

This chapter will review the research findings from brain imaging
techniques focusing on anorexia nervosa and bulimia nervosa,
and categorizing the studies as either structural or functional.
The literature on obesity will also be reviewed, as a substantial
proportion of the obese in weight control programs have bingeeating behaviour (De Zwaan et al., 1994) and are reported to have
many characteristics in common with patients suffering from eating
disorders (Stunkard, 1996).

Tables XXIII-8.1 and XXIII-8.2 present a brief summary of the
studies reviewed in this chapter according to the brain imaging
techniques used.

Numerous important findings in patients with anorexia nervosa were
detected by computed tomography (CT) in studies performed in the
1980s. These structural changes are characterized by an enlargement
of the cortical and cerebellar sulci, the interhemispheric fissure and
the cisterns, and a widening of internal cerebrospinal fluid (CSF)
spaces (Datlof et al., 1986; Lankenau et al., 1985). According to
these studies, as body weight increased, these changes, labelled
'pseudoatrophy' returned to normal (Kohkmeyer, Lemkuhl and
Poutska, 1983; Artmann et al., 1985).

However, there may be different patterns of recovery for the cortical sulci and ventricles over the course of weight restoration. In one of
these studies, 15 anorexic patients out of 25 displayed enlarged ventricles and cortical sulci. After 3 month's treatment, the cortical sulci
returned to normal while the ventricles remained enlarged (Dolan,
Mitchell and Wakeling, 1988). The authors suggested that ventricular enlargement might require longer than 3 months to recover, or
that with sufficient chronicity the observed changes in ventricular
size might be irreversible. The observed reversal of sulcal widening
following refeeding was interpreted as upholding a hypothesis that
the observed changes are secondary to malnourishment.

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